scholarly journals Two Pathway-Specific Transcriptional Regulators, PltR and PltZ, Coordinate Autoinduction of Pyoluteorin in Pseudomonas protegens Pf-5

2021 ◽  
Vol 9 (7) ◽  
pp. 1489
Author(s):  
Qing Yan ◽  
Mary Liu ◽  
Teresa Kidarsa ◽  
Colin P. Johnson ◽  
Joyce E. Loper
Keyword(s):  
Gene Cluster ◽  
Transcriptional Regulator ◽  
Transcriptional Regulators ◽  
Soil Bacterium ◽  
Antibiotic Biosynthesis ◽  
Environmental Cues ◽  
Alternative Mechanism ◽  
Pseudomonas Spp ◽  
Expression Of Genes ◽  
Genes Encoding

Antibiotic biosynthesis by microorganisms is commonly regulated through autoinduction, which allows producers to quickly amplify the production of antibiotics in response to environmental cues. Antibiotic autoinduction generally involves one pathway-specific transcriptional regulator that perceives an antibiotic as a signal and then directly stimulates transcription of the antibiotic biosynthesis genes. Pyoluteorin is an autoregulated antibiotic produced by some Pseudomonas spp. including the soil bacterium Pseudomonas protegens Pf-5. In this study, we show that PltR, a known pathway-specific transcriptional activator of pyoluteorin biosynthesis genes, is necessary but not sufficient for pyoluteorin autoinduction in Pf-5. We found that pyoluteorin is perceived as an inducer by PltZ, a second pathway-specific transcriptional regulator that directly represses the expression of genes encoding a transporter in the pyoluteorin gene cluster. Mutation of pltZ abolished the autoinducing effect of pyoluteorin on the transcription of pyoluteorin biosynthesis genes. Overall, our results support an alternative mechanism of antibiotic autoinduction by which the two pathway-specific transcriptional regulators PltR and PltZ coordinate the autoinduction of pyoluteorin in Pf-5. Possible mechanisms by which PltR and PltZ mediate the autoinduction of pyoluteorin are discussed.

scholarly journals Alopecia in Harlequin mutant mice is associated with reduced AIF protein levels and expression of retroviral elements

2020 ◽  
Author(s):  
Maik Hintze ◽  
Sebastian Griesing ◽  
Marion Michels ◽  
Birgit Blanck ◽  
Lena Wischhof ◽  
...  
Keyword(s):  
Hair Growth ◽  
Transcriptional Regulators ◽  
Mutant Mice ◽  
Wild Type ◽  
Protein Levels ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Keratinocyte Cell ◽  
Apoptosis Inducing Factor ◽  
Hair Cortex

AbstractWe investigated the contribution of apoptosis-inducing factor (AIF), a key regulator of mitochondrial biogenesis, in supporting hair growth. We report that pelage abnormalities developed during hair follicle (HF) morphogenesis in Harlequin (Hq) mutant mice. Fragility of the hair cortex was associated with decreased expression of genes encoding structural hair proteins, though key transcriptional regulators of HF development were expressed at normal levels. Notably, Aifm1 (R200 del) knockin males and Aifm1(R200 del)/Hq females showed minor hair defects, despite substantially reduced AIF levels. Furthermore, we cloned the integrated ecotropic provirus of the Aifm1Hq allele. We found that its overexpression in wild-type keratinocyte cell lines led to down-regulation of HF-specific Krt84 and Krtap3-3 genes without altering Aifm1 or epidermal Krt5 expression. Together, our findings imply that pelage paucity in Hq mutant mice is mechanistically linked to severe AIF deficiency and is associated with the expression of retroviral elements that might potentially influence the transcriptional regulation of structural hair proteins.

scholarly journals Regulation of Polysaccharide Utilization Contributes to the Persistence of Group A Streptococcus in the Oropharynx

2007 ◽  
Vol 75 (6) ◽  
pp. 2981-2990 ◽  
Author(s):  
Samuel A. Shelburne ◽  
Nnaja Okorafor ◽  
Izabela Sitkiewicz ◽  
Paul Sumby ◽  
David Keith ◽  
...  
Keyword(s):  
Parental Strain ◽  
Group A Streptococcus ◽  
Transcriptional Regulator ◽  
Human Saliva ◽  
Transcript Levels ◽  
Expression Of Genes ◽  
Rich Media ◽  
Genes Encoding ◽  
Group A ◽  
Mutant Derivative

ABSTRACT Group A Streptococcus (GAS) genes that encode proteins putatively involved in polysaccharide utilization show growth phase-dependent expression in human saliva. We sought to determine whether the putative polysaccharide transcriptional regulator MalR influences the expression of such genes and whether MalR helps GAS infect the oropharynx. Analysis of 32 strains of 17 distinct M protein serotypes revealed that MalR is highly conserved across GAS strains. malR transcripts were detectable in patients with GAS pharyngitis, and the levels increased significantly during growth in human saliva compared to the levels during growth in glucose-containing or nutrient-rich media. To determine if MalR influenced the expression of polysaccharide utilization genes, we compared the transcript levels of eight genes encoding putative polysaccharide utilization proteins in the parental serotype M1 strain MGAS5005 and its ΔmalR isogenic mutant derivative. The transcript levels of all eight genes were significantly increased in the ΔmalR strain compared to the parental strain, especially during growth in human saliva. Following experimental infection, the ΔmalR strain persistently colonized the oropharynx in significantly fewer mice than the parental strain colonized, and the numbers of ΔmalR strain CFU recovered were significantly lower than the numbers of the parental strain CFU recovered. These data led us to conclude that MalR influences the expression of genes putatively involved in polysaccharide utilization and that MalR contributes to the persistence of GAS in the oropharynx.

scholarly journals Transgene-Induced Silencing of the Zoosporogenesis-Specific NIFC Gene Cluster of Phytophthora infestans Involves Chromatin Alterations

2007 ◽  
Vol 6 (7) ◽  
pp. 1200-1209 ◽  
Author(s):  
Howard S. Judelson ◽  
Shuji Tani
Keyword(s):  
Phytophthora Infestans ◽  
Gene Cluster ◽  
Sequence Similarity ◽  
Transcriptional Regulator ◽  
Hairpin Rna ◽  
High Sequence Similarity ◽  
Genes Encoding ◽  
Cognate Gene ◽  
Chromatin Packing ◽  
Nif Proteins

ABSTRACT Clustered within the genome of the oomycete phytopathogen Phytophthora infestans are four genes encoding spore-specific nuclear LIM interactor-interacting factors (NIF proteins, a type of transcriptional regulator) that are moderately conserved in DNA sequence. NIFC1, NIFC2, and NIFC3 are zoosporogenesis-induced and grouped within 4 kb, and 20 kb away resides a sporulation-induced form, NIFS. To test the function of the NIFC family, plasmids expressing full-length hairpin constructs of NIFC1 or NIFC2 were stably transformed into P. infestans. This triggered silencing of the cognate gene in about one-third of transformants, and all three NIFC genes were usually cosilenced. However, NIFS escaped silencing despite its high sequence similarity to the NIFC genes. Silencing of the three NIFC genes impaired zoospore cyst germination by 60% but did not affect other aspects of the life cycle. Silencing was transcriptional based on nuclear run-on assays and associated with tighter chromatin packing based on nuclease accessibility experiments. The chromatin alterations extended a few hundred nucleotides beyond the boundaries of the transcribed region of the NIFC cluster and were not associated with increased DNA methylation. A plasmid expressing a short hairpin RNA having sequence similarity only to NIFC1 silenced both that gene and an adjacent member of the gene cluster, likely due to the expansion of a heterochromatic domain from the targeted locus. These data help illuminate the mechanism of silencing in Phytophthora and suggest that caution should be used when interpreting silencing experiments involving closely spaced genes.

scholarly journals A widespread family of WYL-domain transcriptional regulators co-localises with diverse phage defence systems and islands

2021 ◽  
Author(s):  
David M Picton ◽  
Joshua D Harling-Lee ◽  
Samuel J Duffner ◽  
Sam C Went ◽  
Richard D Morgan ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Transcriptional Regulator ◽  
Transcriptional Regulators ◽  
Multidrug Resistant ◽  
Common Mechanism ◽  
Defence Mechanisms ◽  
Emerging Pathogen ◽  
Mobility Shift ◽  
Genes Encoding ◽  
Electrophoretic Mobility Shift Assays

Bacteria are under constant assault by bacteriophages and other mobile genetic elements. As a result, bacteria have evolved a multitude of systems that protect from attack. Genes encoding bacterial defence mechanisms can be clustered into 'defence islands', providing a potentially synergistic level of protection against a wider range of assailants. However, there is a comparative paucity of information on how expression of these defence systems is controlled. Here, we functionally characterise a transcriptional regulator, BrxR, encoded within a recently described phage defence island from a multidrug resistant plasmid of the emerging pathogen Escherichia fergusonii. Using a combination of reporters and electrophoretic mobility shift assays, we discovered that BrxR acts as a repressor. We present the structure of BrxR to 2.15 Å, the first structure of this family of transcription factors, and pinpoint a likely binding site for ligands within the WYL-domain. Bioinformatic analyses demonstrated that BrxR homologues are widespread amongst bacteria. About half (48%) of identified BrxR homologues were co-localised with a diverse array of known phage defence systems, either alone or clustered into defence islands. BrxR is a novel regulator that reveals a common mechanism for controlling the expression of the bacterial phage defence arsenal.

scholarly journals A 1,3-1,4-β-Glucan Utilization Regulon in Paenibacillus sp. Strain JDR-2

2016 ◽  
Vol 82 (6) ◽  
pp. 1789-1798 ◽  
Author(s):  
Virginia Chow ◽  
Young Sik Kim ◽  
Mun Su Rhee ◽  
Neha Sawhney ◽  
Franz J. St. John ◽  
...  
Keyword(s):  
Catalytic Domain ◽  
Transcriptional Regulators ◽  
Glycoside Hydrolase Family ◽  
Content Type ◽  
Expression Of Genes ◽  
Paenibacillus Sp ◽  
Genes Encoding ◽  
Marked Preference ◽  
Intracellular Metabolism ◽  
Polymeric Substrates

ABSTRACTPaenibacillussp. strain JDR-2 (PaenibacillusJDR-2) secretes a multimodular cell-associated glycoside hydrolase family 10 (GH10) endoxylanase (XynA10A1) that catalyzes the depolymerization of methylglucuronoxylan (MeGXn) and rapidly assimilates the products of depolymerization. Efficient utilization of MeGXnhas been postulated to result from the coupling of the processes of exocellular depolymerization and assimilation of oligosaccharide products, followed by intracellular metabolism. Growth and substrate utilization patterns with barley glucan and laminarin similar to those observed with MeGXnas a substrate suggest similar processes for 1,3-1,4-β-glucan and 1,3-β-glucan depolymerization and product assimilation. ThePaenibacillusJDR-2 genome includes a cluster of genes encoding a secreted multimodular GH16 β-glucanase (Bgl16A1) containing surface layer homology (SLH) domains, a secreted GH16 β-glucanase with only a catalytic domain (Bgl16A2), transporter proteins, and transcriptional regulators. Recombinant Bgl16A1and Bgl16A2catalyze the formation of trisaccharides, tetrasaccharides, and larger oligosaccharides from barley glucan and of mono-, di-, tri-, and tetrasaccharides and larger oligosaccharides from laminarin. The lack of accumulation of depolymerization products during growth and a marked preference for polymeric glucan over depolymerization products support a process coupling extracellular depolymerization, assimilation, and intracellular metabolism for β-glucans similar to that ascribed to the GH10/GH67 xylan utilization system inPaenibacillusJDR-2. Coordinate expression of genes encoding GH16 β-glucanases, transporters, and transcriptional regulators supports their role as a regulon for the utilization of soluble β-glucans. As in the case of the xylan utilization regulons, this soluble β-glucan regulon provides advantages in the growth rate and yields on polymeric substrates and may be exploited for the efficient conversion of plant-derived polysaccharides to targeted products.

scholarly journals CelR-mediated activation of the cellobiose-utilization gene cluster in Streptococcus pneumoniae

Microbiology ◽  
2011 ◽  
Vol 157 (10) ◽  
pp. 2854-2861 ◽  
Author(s):  
Sulman Shafeeq ◽  
Tomas G. Kloosterman ◽  
Oscar P. Kuipers
Keyword(s):  
Streptococcus Pneumoniae ◽  
Gene Cluster ◽  
Transcriptional Activation ◽  
Sole Carbon Source ◽  
Transcriptional Regulator ◽  
Regulatory Site ◽  
Human Pathogen ◽  
Direct Control ◽  
Atp Binding Cassette Transporters ◽  
Genes Encoding

The human pathogen Streptococcus pneumoniae harbours many genes encoding phosphotransferase systems and sugar ABC (ATP-binding cassette) transporters, including systems for the utilization of the β-glucoside sugar cellobiose. In this study, we show that the transcriptional regulator CelR, which has previously been found to be important for pneumococcal virulence, activates the expression of the cellobiose-utilization gene cluster (cel locus) of S. pneumoniae. Expression directed by the two promoters present in the cel locus was increased in the presence of cellobiose as sole carbon source in the medium, while expression decreased in the presence of glucose in the medium. Furthermore, we have predicted a 22 bp putative CelR regulatory site (5′-YTTTCCWTAWCAWTWAGGAAAA-3′) in the promoters of celA and celB, and in silico analysis showed that it is highly conserved in other pathogenic streptococci as well. Promoter truncations of celA and celB, where the half or full CelR regulatory site was deleted, confirmed that the CelR-binding site in PcelA and PcelB is functional. Transcriptome studies with the celR mutant and in silico prediction of the CelR regulatory site in the entire D39 genome sequence show that the cel locus is the only cluster of genes under the direct control of CelR. Therefore, CelR is a regulator dedicated to the cellobiose-dependent transcriptional activation of the cel locus.

scholarly journals McbG, a LysR Family Transcriptional Regulator, Activates the mcbBCDEF Gene Cluster Involved in the Upstream Pathway of Carbaryl Degradation in Pseudomonas sp. Strain XWY-1

2021 ◽  
Vol 87 (9) ◽  
Author(s):  
Zhijian Ke ◽  
Yidong Zhou ◽  
Wankui Jiang ◽  
Mingliang Zhang ◽  
Hui Wang ◽  
...  
Keyword(s):  
Binding Site ◽  
Gene Cluster ◽  
Transcriptional Activation ◽  
Regulatory Mechanism ◽  
Hydrolysis Product ◽  
Transcriptional Regulator ◽  
Transcriptional Regulators ◽  
Palindromic Sequence ◽  
Mobility Shift ◽  
Lysr Family

ABSTRACT Although enzyme-encoding genes involved in the degradation of carbaryl have been reported in Pseudomonas sp. strain XWY-1, no regulator has been identified yet. In the mcbABCDEF cluster responsible for the upstream pathway of carbaryl degradation (from carbaryl to salicylate), the mcbA gene is constitutively expressed, while mcbBCDEF is induced by 1-naphthol, the hydrolysis product of carbaryl by McbA. In this study, we identified McbG, a transcriptional activator of the mcbBCDEF cluster. McbG is a 315-amino-acid protein with a molecular mass of 35.7 kDa. It belongs to the LysR family of transcriptional regulators and shows 28.48% identity to the pentachlorophenol (PCP) degradation transcriptional activation protein PcpR from Sphingobium chlorophenolicum ATCC 39723. Gene disruption and complementation studies reveal that mcbG is essential for transcription of the mcbBCDEF cluster in response to 1-naphthol in strain XWY-1. The results of the electrophoretic mobility shift assay (EMSA) and DNase I footprinting show that McbG binds to the 25-bp motif in the mcbBCDEF promoter area. The palindromic sequence TATCGATA within the motif is essential for McbG binding. The binding site is located between the –10 box and the transcription start site. In addition, McbG can repress its own transcription. The EMSA results show that a 25-bp motif in the mcbG promoter area plays an important role in McbG binding to the promoter of mcbG. This study reveals the regulatory mechanism for the upstream pathway of carbaryl degradation in strain XWY-1. The identification of McbG increases the variety of regulatory models within the LysR family of transcriptional regulators. IMPORTANCE Pseudomonas sp. strain XWY-1 is a carbaryl-degrading strain that utilizes carbaryl as the sole carbon and energy source for growth. The functional genes involved in the degradation of carbaryl have already been reported. However, the regulatory mechanism has not been investigated yet. Previous studies demonstrated that the mcbA gene, responsible for hydrolysis of carbaryl to 1-naphthol, is constitutively expressed in strain XWY-1. In this study, we identified a LysR-type transcriptional regulator, McbG, which activates the mcbBCDEF gene cluster responsible for the degradation of 1-naphthol to salicylate and represses its own transcription. The DNA binding site of McbG in the mcbBCDEF promoter area contains a palindromic sequence, which affects the binding of McbG to DNA. These findings enhance our understanding of the mechanism of microbial degradation of carbaryl.

scholarly journals Mitochondrial DNA Instability in Cells Lacking Aconitase Correlates with Iron Citrate Toxicity

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Muhammad A. Farooq ◽  
Tammy M. Pracheil ◽  
Zhejun Dong ◽  
Fei Xiao ◽  
Zhengchang Liu
Keyword(s):  
Mitochondrial Dna ◽  
Citrate Synthase ◽  
Tricarboxylic Acid Cycle ◽  
Alternative Mechanism ◽  
Iron Citrate ◽  
Expression Of Genes ◽  
Genes Encoding ◽  
Citrate Accumulation ◽  
Mitochondrial Dna Instability ◽  
Mutant Cells

Aconitase, the second enzyme of the tricarboxylic acid cycle encoded byACO1in the budding yeastSaccharomyces cerevisiae, catalyzes the conversion of citrate to isocitrate.aco1Δ results in mitochondrial DNA (mtDNA) instability. It has been proposed that Aco1 binds to mtDNA and mediates its maintenance. Here we propose an alternative mechanism to account for mtDNA loss inaco1Δ mutant cells. We found thataco1Δ activated the RTG pathway, resulting in increased expression of genes encoding citrate synthase. By deletingRTG1,RTG3, or genes encoding citrate synthase, mtDNA instability was prevented inaco1Δ mutant cells. Increased activity of citrate synthase leads to iron accumulation in the mitochondria. Mutations inMRS3andMRS4, encoding two mitochondrial iron transporters, also prevented mtDNA loss due toaco1Δ. Mitochondria are the main source of superoxide radicals, which are converted to H2O2through two superoxide dismutases, Sod1 and Sod2. H2O2in turn reacts with Fe2+to generate very active hydroxyl radicals. We found that loss of Sod1, but not Sod2, prevents mtDNA loss inaco1Δ mutant cells. We propose that mtDNA loss inaco1Δ mutant cells is caused by the activation of the RTG pathway and subsequent iron citrate accumulation and toxicity.

Sign in / Sign up

Export Citation Format

Share Document